Is there a correlation between ventricular fibrillation cycle length and electrophysiological and anatomic properties of the canine left ventricle?

2004 ◽  
Vol 287 (2) ◽  
pp. H823-H832
Author(s):  
Taresh Taneja ◽  
George Horvath ◽  
Darlene K. Racker ◽  
David Johnson ◽  
Jeffrey Goldberger ◽  
...  
Author(s):  
Nicholas Tan ◽  
Georgios Christopoulos ◽  
Thomas P. Ladas ◽  
Zhi Jiang ◽  
Alan M. Sugrue ◽  
...  

Background: Rigorous study of ventricular fibrillation (VF) is not feasible in humans. The spatiotemporal characteristics of prolonged VF remain undefined, limiting our understanding of this lethal rhythm. Methods: VF was mapped in 4 canines. The endocardial and epicardial left ventricle (LV) and right ventricle (RV) were sequentially mapped at 0 to 15, 15 to 30, 30 to 45, and 45 to 60 minutes post-induction. Ten consecutive beats were used to determine average cycle length and regularity index of ventricular and His-Purkinje system signals in discrete regions during each time interval. Results: Average VF time was 58±12 minutes. The shortest ventricular cycle length was present in the RV apical region (70±10 msec) at 0 to 15 minutes and at 15 to 30 minutes (89±31 msec) and LV apical region at 45 to 60 minutes (242±163 msec). The His-Purkinje system cycle length was the shortest at the RV outflow tract (75±3 msec) at 0 to 15 minutes, RV inflow and free wall (89±12 msec) at 15 to 30 minutes, LV apical region (83±14 msec) at 30 to 45 minutes, and inferior and inferolateral LV (145±23 msec) at 45 to 60 minutes. Regularity index was the highest in the RV inflow and free wall (78%) at 0 to 15 minutes, RV apical region (86%) at 15 to 30 minutes, LV septum and epicardial anterior RV (80%) at 30 to 45 minutes, and anterior and anterolateral LV (75%) at 45 to 60 minutes. Conclusions: These data suggest significant regional changes in electrical activity throughout VF in canines. A transition of fastest electrical activity from RV to LV apical regions across VF was observed. Further studies are warranted to confirm the above findings.


1961 ◽  
Vol 201 (3) ◽  
pp. 457-461 ◽  
Author(s):  
Robert A. vanTyn ◽  
Lloyd D. MacLean

The use of single rectangular stimuli, applied directly to the heart surface, has been confirmed as a reliable method for measurement of the ventricular fibrillation threshold (VFT). The following factors which influence reproducibility were investigated: 1) spatial separation of bipolar electrodes, 2) interval between stimuli, and 3) anatomical position of electrodes on the heart. With bipolar electrodes placed 10–30 mm apart and an interval of 10–15 cycles between stimuli the VFT was remarkably constant for any single dog. An interelectrode separation of 2–4 mm or the placement of electrodes in a coagulated area of epicardium produced high, widely variable, and at times unobtainable thresholds believed due to short circuiting of the current delivered. Thresholds determined with stimuli 3–4 beats apart were significantly lower than when stimuli were delivered 10–15 beats apart. The VFT was significantly higher at the base than at the apex of the left ventricle. Investigations which measure the effect of a given influence on the VFT should control the factors studied here.


2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.


1998 ◽  
Vol 274 (4) ◽  
pp. H1113-H1120 ◽  
Author(s):  
Michael R. Ujhelyi ◽  
J. Jason Sims ◽  
Allison Winecoff Miller

This study assessed the effect of low (10 mg ⋅ kg−1 ⋅ h−1) and very high (18 mg ⋅ kg−1 ⋅ h−1) doses of lidocaine on defibrillation energy requirements (DER) to relate changes in indexes of sodium-channel blockade with changes in DER values using a dose-response study design. In group 1 (control; n = 6 pigs), DER values were determined at baseline and during treatment with 5% dextrose in water (D5W) and with D5W added to D5W. In group 2 ( n = 7), DER values were determined at baseline and during treatment with low-dose lidocaine followed by high-dose lidocaine. In group 3 ( n = 3), DER values were determined at baseline and high-dose lidocaine. Group 3 controlled for the order of lidocaine treatment with the addition of high-dose lidocaine after baseline. DER values in group 1 did not change during D5W. In group 2, low-dose lidocaine increased DER values by 51% ( P = 0.01), whereas high-dose lidocaine added to low-dose lidocaine reduced DER values back to within 6% of baseline values ( P = 0.02, low dose vs. high dose). DER values during high-dose lidocaine in group 3 also remained near baseline values (16.2 ± 2.7 to 12.9 ± 2.7 J), demonstrating that treatment order had no impact on group 2. Progressive sodium-channel blockade was evident as incremental reduction in ventricular conduction velocity as the lidocaine dose increased. Lidocaine also significantly increased ventricular fibrillation cycle length as the lidocaine dose increased. However, the greatest increase in DER occurred when ventricular fibrillation cycle length was minimally affected, demonstrating a negative correlation ( P = 0.04). In summary, lidocaine has an inverted U-shaped DER dose-response curve. At very high lidocaine doses, DER values are similar to baseline and tend to decrease rather than increase. Increased refractoriness during ventricular fibrillation may be the electrophysiological mechanism by which high-dose lidocaine limits the adverse effects that low-dose lidocaine has on DER values. However, there is a possibility that an unidentified action of lidocaine is responsible for these effects.


2002 ◽  
Vol 39 ◽  
pp. 92
Author(s):  
Taresh Tanela ◽  
George Horvath ◽  
Darlene Racker ◽  
Jeffrey Goldberger ◽  
Alan Kadish

Heart Rhythm ◽  
2005 ◽  
Vol 2 (7) ◽  
pp. 720-728 ◽  
Author(s):  
Jian Huang ◽  
Greg P. Walcott ◽  
Cheryl R. Killingsworth ◽  
Sharon B. Melnick ◽  
Jack M. Rogers ◽  
...  

2007 ◽  
Vol 293 (6) ◽  
pp. H3506-H3516 ◽  
Author(s):  
Jonathan M. Cordeiro ◽  
Jane E. Malone ◽  
José M. Di Diego ◽  
Fabiana S. Scornik ◽  
Gary L. Aistrup ◽  
...  

Previous studies indicate that action potential duration (APD) alternans is initiated in the endocardial (END) and midmyocardial (MID) regions rather than the epicardium (EPI) in the canine left ventricle (LV). This study examines regional differences in the rate dependence of Ca2+ transient characteristics under conditions that give rise to APD and associated T wave alternans. The role of the sarcoplasmic reticulum (SR) was further evaluated by studying Ca2+ transient characteristics in myocytes isolated from neonates, where an organized SR is poorly developed. All studies were performed in cells and tissues isolated from the canine LV. Isolated canine ENDO, MID, and EPI LV myocytes were either field stimulated or voltage clamped, and Ca2+ transients were measured by confocal microscopy. In LV wedge preparations, increasing the basic cycle length (BCL) from 800 to 250 ms caused alternans to appear mainly in the ENDO and MID region; alternans were not observed in EPI under these conditions. Ca2+ transient alternans developed in response to rapid pacing, appearing in EPI cells at shorter BCL compared with MID and ENDO cells (BCL=428 ± 17 vs. 517 ± 29 and 514 ± 21, respectively, P < 0.05). Further increases in pacing rate resulted in the appearance of subcellular alternans of Ca2+ transient amplitude, which also appeared in EPI at shorter BCL than in ENDO and MID cells. Ca2+ transient alternans was not observed in neonate myocytes. We conclude that 1) there are distinct regional differences in the vulnerability to rate-dependent Ca2+ alternans in dog LV that may be related to regional differences in SR function and Ca2+ cycling; 2) the development of subcellular Ca2+ alternans suggests the presence of intracellular heterogeneities in Ca2+ cycling; and 3) the failure of neonatal cells to develop Ca2+ alternans provides further support that SR Ca2+ cycling is a major component in the development of these phenomena.


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